Heparin anticoagulation is essential during hemodialysis. The frequency of heparin-induced thrombocytopenia (HIT) during the initial phase of dialysis treatment is known to be 3.8%. In North America and Europe, an algorithmic approach to HIT diagnosis including the 4T scoring system has been developed. A standard diagnostic procedure in combination with a screening enzyme immunoassay that detects platelet factor 4/heparin complex antibodies (HIT antibodies) and a confirmatory test using ¹⁴C serotonin release assay has been established. In Japan, two chemiluminescence assays and a latex agglutination test have been approved for detecting HIT antibodies in suspected HIT patients. However, there have only been a few published papers about these tests, and their clinical benefit has not been fully elucidated. Also, little is known about how the three tests to contribute to HIT diagnosing in hemodialysis patients, and there is no evidence that the tests have the same ability to diagnose HIT as classical standard of enzyme immunoassays. Therefore, precise assessments of the 4T scoring system are critical for diagnosing HIT before HIT antibody test is performed in hemodialysis patients. In dialysis patients suffering from extracorporeal circuit clotting, an appropriate HIT diagnosis can be obtained by the addition to one point as thrombosis in the 4T scoring system.

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The case of a 64-year-old man who started hemodialysis at the age of 31 years is presented. The patient began experiencing diarrhea in July 2013 and presented with a circumferential protruding lesion and an ulcer in the ascending colon. An examination of the biopsy sample showed inflammatory cell infiltration. The patient revealed a positive result of an interferon-γ release assay test and was diagnosed with intestinal tuberculosis. Treatment with antituberculous drugs was initiated, but was ineffective. Four months later, the patient also developed ileus and consequently underwent right hemicolectomy, ileostomy, and mucous fistula. Postoperatively, the patient exhibited hypotension, hyperkalemia, and metabolic acidosis. The cause of the acidosis was considered to be massive diarrhea, and it improved after the administration of sodium bicarbonate and other treatments. However, the hyperkalemia persisted even after ion-exchange resin treatment. One year later, a stoma reversal was performed, and the patient’s serum potassium level subsequently decreased. As his hyperkalemia improved promptly after the stoma reversal, it was considered that it had been caused reduced potassium excretion in the colon. This case highlights the importance of a compensatory mechanism for increasing intestinal potassium excretion in hemodialysis patients.

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This case involved a 30-year-old woman. She had exhibited a urinary abnormality during a medical check-up more than 10 years earlier, but it had been left untreated. In February 2014, she felt a scratching sensation around her eyelid and visited a local ophthalmological department in May of that year. She was treated with eye drops and ointment, but her condition did not improve, and so it was suspected that she was suffering from a disease affecting another part of her body. At the end of May, she visited a local internal medicine department, where she was diagnosed with a suspected acute kidney injury. As a result, she was referred to our hospital, where she was subsequently hospitalized. She was diagnosed with end-stage renal disease, and so peritoneal dialysis was started. The patient had previously exhibited paramenia and had been experiencing amenorrhea for the past three years. She was subsequently diagnosed with polycystic ovary syndrome based on blood and ultrasound examinations and was treated with Kaufmann therapy, which resulted in remission. Clinicians should be aware that amenorrhea can be caused by gynecological disease, which can often be treated, as well as renal failure when treating women of reproductive age with suspected renal failure.

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This study describes the case of an 84-year-old Japanese male who had been on maintenance hemodialysis for 3 years and was examined for gradually worsening hypercalcemia (corrected serum calcium level, 13.1 mg/dL). Although cultures of his sputum and gastric juice specimens did not show any evidence of Mycobacterium, positron emission tomography-computed tomography (CT) revealed lymphadenopathy in the pulmonary hila and mediastinum. A high value was also obtained during the QuantiFERON^® TB-2G test (3.04 IU/mL). Moreover, the patient’s 1,25-dihydroxyvitamin D (1,25(OH)₂D) to intact parathyroid hormone (i-PTH) serum level ratio was high (6.75 pg/pg). The patient was clinically diagnosed with hypercalcemia, which was suspected to have been caused by a tuberculosis infection, and was treated with antituberculous medications. After 6 months of therapy, his corrected serum calcium level had decreased to 8.7 mg/dL, and his 1,25(OH)₂D to i-PTH serum level ratio had fallen to 0.04. A marked reduction in the size of the patient’s lymph nodes was observed on CT. The diagnosis of tuberculosis in cases involving atypical presentations such as extrapulmonary involvement is often difficult, and it may be necessary to start antituberculous therapy without a definite diagnosis in such cases. The low 1,25(OH)₂D to i-PTH serum level ratios seen in hemodialysis patients are presumed to be due to a combination of disordered vitamin D metabolism and secondary hyperparathyroidism. In general, hemodialysis patients with granulomatous disease have higher serum levels of 1,25(OH)₂D, which is synthesized in granulomas outside the kidneys, thereby leading to lower serum levels of i-PTH. In the present case, the patient’s high 1,25(OH)₂D to i-PTH serum level ratio gradually decreased following the administration of antituberculous therapy. Thus, the 1,25(OH)₂D to i-PTH serum level ratio aided the diagnosis of tuberculosis and the evaluation of the therapeutic response to antituberculous medication in a hemodialysis patient with hypercalcemia.

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A 26-year-old female walked into our emergency department complaining of persistent nausea and feeling unwell after ingesting about 100 mL laundry detergent in a suicide attempt. The laundry detergent contained 17% of anionic and non-ionic surfactants. She had airway and breathing problems on arrival. We intubated her and performed gastric lavage, before administering activated charcoal and a laxative. We continued the infusion, but her blood lactate level kept rising, and progressive circulatory failure was observed. She fell into a state of shock, and we needed to use noradrenaline. We decided to perform direct hemoperfusion (DHP) using an activated charcoal column. After the initiation of the DHP, the patient’s blood lactate level fell immediately, and we were able to end the noradrenaline treatment. She was extubated on the 3rd hospital day and transferred to another hospital for specialized psychiatric treatment on the 17th hospital day. Although blood purification therapy for acute intoxication is controversial, we herein report a case of surfactant poisoning in which DHP was considered to have contributed to the improvement of circulatory failure.

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A 72-year-old male, who had been undergoing peritoneal dialysis due to end-stage renal failure caused by nephrosclerosis for 15 months, consulted our outpatient department because he had suffered watery diarrhea and had subsequently noticed that his peritoneal dialysate was cloudy. He was diagnosed with peritonitis based on the detection of an increased leukocyte count in his dialysate. He was admitted to hospital, and empiric antibiotic treatment was initiated although culture tests produced negative results. The patient’s peritonitis and the cloudiness of his dialysate soon improved and so he was discharged within 10 days. However, on the day of discharge his dialysate became cloudy again, and he had to be re-hospitalized. This time, a culture of his dialysate fluid revealed an aerobic Gram-negative bacillus, which was identified as Paracoccus yeei. Suitable antibiotic treatment with ceftazidime was administered for 21 days, and the patient made an uneventful recovery. Paracoccus yeei, a newly-discovered Gram-negative coccobacillus that was first detected in 2003, rarely causes peritonitis, but Paracoccus yeei-induced peritonitis can be successfully treated once the etiological agent has been elucidated.

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An 89-year-old female was admitted to our hospital as an emergency case on Dec X, 201X. She presented with acute pyelonephritis, septic shock, and atrial fibrillation. On admission, heparin was administered for atrial fibrillation. On Day 2, hemodialysis was initiated due to worsening renal failure using a double lumen catheter inserted into the common iliac vein. By Day 3, the catheter had become occluded. Thus, it was removed, and another double lumen catheter was inserted in the internal jugular vein for hemodialysis. By Day 4, the double lumen catheter had become occluded again. On Day 9, venous thrombosis was detected, and a filter was inserted into the inferior vena cava. At that time, it was found that the patient’s platelet count had decreased from 13.4×10⁴/μL to 6.2×10⁴/μL. Type Ⅱ heparin-induced thrombocytopenia (HIT) was suspected, and so the heparin was discontinued, and argatroban therapy was initiated. Two days later, warfarin treatment was also started. On Day 25, peritoneal dialysis was initiated because it was difficult to maintain venous access during hemodialysis, despite the administration of warfarin therapy. A test for HIT antibody produced a positive result (1.3 U/mL). In this case, early onset platelet depletion and venous thrombosis occurred 4 days after the initiation of heparin therapy. In cases of atypical onset HIT, clinicians should consider the possibility of acute-onset or spontaneous HIT.

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